Endotoxin is a polysaccharide derived from the cell wall of gram negative bacteria. When injected into the footpad or the eye of a rat it will induce an inflammatory reaction within the eye. The mechanism of this inflammation is still unclear. However, since several types of anterior uveitis in humans appear to be linked to gram negative bacteria exposure, this is considered a relative model for anterior uveitis in humans such as Reiter's syndrome. In this study the expression of class II antigens was studied within the eyes of rats receiving E. coli endotoxin by immunohistochemical techniques. We observe that the expression of class II antigens on the ciliary body and iris preceded the influx of inflammatory cells into the eye and that the inflammatory cells that entered the eye were primarily neutrophils with some monocytes. No T-cells were present in the inflammatory infiltrate. The inflammatory cellular infiltrate could be inhibited by indomethacin or colchicine, however this did not alter the expression of class II antigens by the iris or ciliary body indicating that this expression is not simply a consequence of the inflammatory infiltrate but may be intimately involved with the mechanism of the expression of endotoxin induced uveitis. Corticosteroids were capable of suppressing both the cellular inflammatory infiltrate and the expression of class II antigens. The expression of class II antigens on nonlymphoid cells within the eye may be important in antigen presentation or may simply signal a phenotypic change on the cells due to the interaction of endotoxin with the cell membranes. The findings were compared with the expression of class II antigen in passive and active intraocular Arthus. The effect of endotoxin on ocular inflammation was studied using fluorophotometry to validate the use of animal studies as a useful